Pharmacology in Pain Management Flashcards
mild pain
(1-3)
-use step 1 drugs (NSAIDS & acetaminophen)
pain is a reflection of what?
emotion and attitude
R: region
where is it? does it stay there?
treatments
-2nd line:
Tryptans are serotonin/ 5-HT-1 receptors against that constrict intracranial vessels.
sumatriptans, zolmitriptan, rizatriptan, etc. (have various half-lives, times of onset)
some also come in combo, sumatriptan plus naproxin
tension headaches
- dull quality, pain radiates to forehead, neck, shoulders
how do we assess pain?
PQRSTU
severe pain
(7-10)
-use opiates/ step 3 (morphine, hydromorphone/dilaudid, oxycodone/oxycontin, oxymorphone, Fentora)
Local anesthetics
sodium channel blockers that reduce pain impulses (novocaine)
(lidocaine)
transmission
through dorsal horn of cord; if signal is strong enough, may reach CNS, though there are inhibitory fibers in cord to reduce upstream signal
treatment of tension headache
- acetaminophen & aspirin (1st line)
- NSAIDS (2nd line)
- can give antiemetics if accompanying nausea (promethazine/ prochlorperazine)
- combination of meds: (3rd line)
- Fioricet (butalbital/ acetaminophen/ caffeine)
- Fiorinal (butalbital/ aspirin/ caffeine)
- *** some anti-depressants also used, including amitriptyline, fluoxetine, others
chronic pain:
- lasts over 3-6 months
- pain persists after injury has healed
- can be from a variety of tissues
- perhaps the result of “neuroplasticity”
anti-convulsants
gabapentin & pregabalin activate GABA receptors & reduce neutotransmitters
acute pain
sudden onset & related to a specific case (trauma/damage)
- can be accompanied by other physiological responses, (increased HR, sweating, rapid breathing)
Treating pain
mild pain
moderate pain
severe pain
what is pain?
Unpleasant sensory & emotional experience associated w/ actual or potential tissue damage
signal reducers
those that normally inhibit pain signals
-B-endorphin (mu receptors), NE, and GABA
what is pain pathophysiology?
transduction
transmission
perception
modulation
mediators or pain signals
PG’s, substance P (even stimulating second order neurons in cord)
bradykinins
P: precipitating/ palliating
what makes it worse or better?
treatments
-3rd line: Ergot derivatives (ergotamine or dihydroergotamine) lead to vasoconstriction
Co-Analgesics for pain
Antidepressants
Anticonvulsants
Local Anesthetics
Muscle Relaxants
Migraine triggers?
- physiologic factors(anxiety, depression)
- medications (hormones, nicotine, nitroglycerin)
- diet (alcohol, caffeine, chocolate)
- environment (light, altitude, odors, sounds, weather)
- lifestyle (dieting, exercise, sleep patterns)
- hormonal factors (pregnancy, menopause)
transduction
A-delta nerves and C-nerves (fibers) are activated by PGs, substance P, histamine, etc
modulation
inhibitory effects in the CNS to reduce the sense of pain in a descending pathway
moderate pain
(4-6)
-use NSAIDS plus opiates/ step 2 (hydrocodone/Vicodin, oxycodone/Percocet)
S: severity
Pain scales?
treatments
-1st line:
(NSAIDS & aspirin)
caffeine- containing meds (Excedrin (migraine))
perception
signals in both the cortex and limbic system
=
COGNITIVE & EMOTIONAL component
cluster headaches
disabling, burning, or boring feeling around one eye & extremely painful
migraine
head throbbing, nausea, photophobia, photophobia, and can be debilitating
Headaches
tension headaches
migraines
cluster headaches
anti-depressants
tricyclics & SNRI will reduce NE uptake & help reduce neurotransmitters in nociception (amitriptyline & venlafaxine)
chronic pain
LONG-LIVED acute pain where patients can accommodate to the physiological response
- CAN OFTEN LEAD TO DEPRESSION AND ANXIETY
what causes migraine headaches?
- can be genetic somewhat, often associated w/ LOW estrogen levels
- thought to be vascular (too much vasodilation in cranial vessels)
but NOW, believed to be more neurogenic, involving neurons from the trigeminal nerve leading to vasodilation of meningeal blood vessels, release of inflammatory agents, more dilation, then headache
what causes tension headaches?
- thought to be due to muscle tone in pericardial region
- often associated with sleep deprivation, smoking, cessation
- if treated too often, can lead to MOH (medication Overuse Headache)
types of pain
nociceptive
neuropathic
acute
chronic
Q: quality
what does it feel like?
T: temporal patterns
is it constant? intermittent?
Prophylaxis of migraines
- 1st line: Beta blockers (propanolol, metoprolol, atenolol, etc) or tricyclic
antidepressants (imipramine, nortriptyline, amitriptyline)
anticonvulsants (valproic acid, topiramate)
Calcium Channel Blockers
neuropathic pain
from CNS processing following insult from disease or trauma such as:
tingling, burning, shooting, etc.,
Muscle relaxants
likely only used when pain is related to muscle spasm
Rescue agent?
opioids such as: butorphanol or codeine can be used
U: you
how does it affect you?
nociceptive pain
from stimulation of neurons following injury, disease of inflammation of tissue
- can be somatic (muscle, skin, or bone associated)
- can be visceral (organ associated)
